Infectious Diseases I: Viral Infections (V1) - PDF

PATHOLOGY | TRANS #4A LE Infectious Diseases I: Viral Infections DR. ARLENE SANTOS | Lecture Date (09/27/2024) |...

PATHOLOGY | TRANS #4A LE Infectious Diseases I: Viral Infections DR. ARLENE SANTOS | Lecture Date (09/27/2024) | Version #1 02 OUTLINE → Involved in T-cell activation I. Types of Viral Infections IV. Chronic Nectin-4 II. Acute Infections Productive/Persistent → Found on the basal surface of epithelial cells A. Measles Infections → Important for viral replication within the respiratory tract B. Mumps V. Transforming Viral C. Dengue Infections PATHOGENESIS OF MEASLES III. Latent Infections A. EBV GENERAL A. HSV VI. Review Questions The measles virus can disseminate to many tissues B. VZV VII. References including: C. CMV → Skin, conjunctiva Must Lecturer Book Previous Youtube → Respiratory tract ❗️ Know 💬 📖 📋 Trans Video 🔺 → Urinary tract → Small blood vessels & lymphatic system SUMMARY OF ABBREVIATIONS → CNS Most children develop T-cell mediated immunity to CO Class Officer measles virus that helps control the infection & produces HSV Herpes Simplex Virus the measles rash CMV CytomegaloVirus In malnourished children, measles may cause any of HIV Human Immunodeficiency Virus these: HBV Hepatitis B Virus → Croup EBV Epstein-barr Virus ▪ Upper airway infection, narrowing, and barking-like HPV Human papillomavirus cough LEARNING OBJECTIVES → Pneumonia → Diarrhea with protein-losing enteropathy ✔ General characteristics of the pathogen → Keratitis with scarring & blindness ✔ Pathogenesis of the disease → Encephalitis ✔ Characteristic macroscopic and microscopic findings → Hemorrhagic rashes seen in the disease ✔ Overview of the characteristic clinical findings and STEPS IN THE PATHOGENESIS common laboratory tests used to diagnose the infections 1. Transmitted by the airborne route through aerosolized and diseases respiratory secretions I. TYPES OF VIRAL INFECTIONS 2. Viral multiplication within the respiratory tract Table 1. Types of Viral Infection 3. Spreads into local lymphoid tissues 4. Viremia Type of Infection Virus 5. Systemic dissemination to many tissues Acute (Transient) Measles, Mumps, Poliovirus, Infection Dengue virus PATHOLOGIC FINDINGS IN MEASLES ❗ Latent Infections HSV, Varicella-zoster virus (VZV), GROSS PATHOLOGY IN MEASLES CMV Blotchy, reddish brown rash on the face, trunk & Chronic HIV, HBV proximal extremities, produced by dilated blood Productive vessels (Persistent Virus-infected cells in capillaries & blood vessels are Infections) recognized by the immune-reactive T-lymphocytes Transforming EBV, HPV, HBV B&C → Less frequent in people with cell-mediated immunity Viral infections deficiencies Rash is an immune reaction (T-cell mediated immunity) to II. ACUTE (TRANSIENT INFECTIONS) the viral antigen Viruses that cause transient infections, in general, elicit Rash occurs originally on the face, behind the ears & the effective immune responses that eliminate the pathogens, neck which then spreads to the trunk & extremities thereby limiting the duration of these infections. A. MEASLES GENERALITIES A single stranded RNA virus (ssRNA) → Can replicate in a variety of cell types including epithelial cells and leukocytes Cell surface receptors: → CD 46: complement regulatory protein that inactivates C3 convertases Signaling Lymphocytic Activation Molecule → Expressed on activated lymphocytes, dendritic cells Figure 1. Left: Rash-Face. Right: Rase-Face & Trunk[Lecturer’s PPT] & monocytes → Initial receptor of the virus LE 1 TG 1 | L. Oronce, M. Ostoy, A. Pabunan, D. Padrigone, & TE | L. Ponio, S. Rivera AVPAA | R. Sabado PAGE 1 of 10 TRANS 1 R. Pajaro VPAA | D. Patajo  PATHOLOGY | LE 1 Infectious Disease I: Viral infections| Dr. Arlene Santos Prodromal stage: marked by the symptoms of cough, MICROSCOPIC PATHOLOGY IN MEASLES coryza (colds), and conjunctivitis (3C’s) Microscopically: dilated skin vessels, edema, and → Accompanied by fever which rises steadily until the mononuclear perivascular inflammatory infiltrate appearance of the rash 2-4 days later Lymphoid organs → Progression: 3Cs + fever → rash → Microscopically::follicular hyperplasia, large germinal centers ▪ Warthin-Finkelday cells (pathognomonic) − Large multinucleated giant cells with eosinophilic, nuclear and cytoplasmic inclusion bodies − Found in the lymphoid organs, lungs, and sputum Measles pneumonia → Microscopically: peribronchial & Interstitial mononuclear infiltration Figure 2. Left (Eyes after 3 days): The child has watery eyes, which are a manifestation of conjunctivitis. Right (Eyes & Nose): The child has watery eyes and nasal discharge[Lecturer’s PPT] ❗ Koplik’s spots → Ulcerated mucosal lesions in the oral cavity near the opening of the Stensen’s duct → In the oral cavity (lateral buccal mucosa & upper lip but may also involve the entire inner mouth) → Pathognomonic of measles → Microscopically, Koplik’s spots are: ▪ Necrosis ▪ Neutrophilic exudate ▪ Neovascularization Figure 5. Upper image: measles multinucleated giant cells (Warthin-Finkeldey cells) in the lung. Lower image: Warthin-Finkeldey bodies in the lymph nodes[Lecturer’s PPT]. Figure 3. Koplik Spots[Lecturer’s PPT] Figure 6. Image of the lung taken from a patient with measles pneumonia. The normal alveolar architecture has been obliterated (note the presence of the Warthin-Finkeldey cell)[Lecturer’s PPT] Other microscopic findings: → Follicular hyperplasia → Large germinal centers Figure 4. Child with measles rash & conjunctivitis[Lecturer’s PPT] PATHOLOGY Infectious Diseases I: Viral Infections PAGE 2 of 10 PATHOLOGY | LE 1 Infectious Disease I: Viral infections| Dr. Arlene Santos B. MUMPS MICROSCOPIC PATHOLOGY IN MUMPS Acute systemic viral infection usually associated with Edematous interstitium of the parotid gland is diffusely swelling and pain of the salivary gland infiltrated by lymphocytes, macrophages, and plasma Transient infection caused by Mumps virus cells which compresses the acini and ducts → Enters into the respiratory tract through inhalation of Neutrophils and necrotic debris may fill the lumen of the respiratory droplets ducts → result to focal damage to the lining epithelium of → Spreads to draining lymph nodes the ducts → Replicates in T-lymphocytes Hematogenous spread to organs C. DENGUE → Salivary glands: mumps parotitis Viral hemorrhagic fever → CNS: mumps encephalitis Severe, life threatening, multi-system syndrome in ▪ Microscopic findings: perivenous demyelination, which there is vascular damage leading to widespread perivascular mononuclear cuffing hemorrhage and shock → Pancreas: acute pancreatitis Caused by Flavivirus (serotypes 1 - 4) ▪ Acinar cell injury → release of digestive enzymes → Transmitted by mosquito bite (Aedes aegypti) parenchymal necrosis and fat necrosis → neutrophil Infects mononuclear phagocytes and hepatocytes rich inflammation Clinical symptoms: → Testis: mumps orchitis → Headache, fever ▪ Microscopic findings: edema, mononuclear → Myalgia infiltration, focal hemorrhages → Joint pain − May compromise blood supply which leads to → Conjunctival congestion, retro-orbital pain with infarction (necrosis) → scarring (fibrosis) → generalized transient macular rash atrophy and sterility → Mild to severe hemorrhage → Ovaries: mumps oophoritis → Shock PATHOLOGIC FINDINGS IN MUMPS DENGUE HEMORRHAGIC FEVER GROSS PATHOLOGY IN MUMPS A variant and more severe form of dengue fever Mumps virus infects ductal epithelial cells of salivary Associated with: gland → Hypoproteinemia → Swollen neck region due to enlarged salivary glands → Thrombocytopenia → Bilateral involvement in 70% of cases → Prolonged bleeding time → Results in: → Elevated prothrombin time ▪ Desquamation of involved cells → edema → PATHOLOGIC FINDINGS IN DENGUE FEVER inflammation → pain and swelling Diagnosis → Clinical history → Hemoconcentration → Leukopenia with lymphocytosis → Thrombocytopenia → Serological tests GROSS PATHOLOGY IN DENGUE FEVER Conjunctival hemorrhage → Pinpoint areas of bleeding Figure 7. Bilateral swelling of the parotid glands [Lecturer’s PPT] → Combination of: ▪ Thrombocytopenia, platelet dysfunction MUMPS PAROTITIS ▪ Endothelial injury Bilateral swelling of the parotid glands ▪ Cytokine-induced disseminated intravascular Enlarged, doughy, moist and reddish brown coagulation (DIC) ▪ Deficiency of clotting factors due to hepatic injury Maculopapular or Scarlatiniform Rash → Initial manifestation: ▪ Petechiae ▪ Epistaxis or mucosal bleeding (possible) → Typically begins on the 3rd or 4th day → May last for 24 to 72 hours → Fades with desquamation Figure 8. Bilateral swelling of the parotid glands [Lecturer’s PPT] Figure 9. Conjunctival hemorrhage (yellow arrow)[Lecturer’s PPT]. PATHOLOGY Infectious Diseases I: Viral Infections PAGE 3 of 10 PATHOLOGY | LE 1 Infectious Disease I: Viral infections| Dr. Arlene Santos ❗ HSV1 A. HERPES SIMPLEX VIRUS (HSV) and HSV2 can cause cutaneous and genital 📋 lesions. 📋 → HSV-1: commonly cause oral lesions → HSV-2: commonly cause genital lesions HSV causes focal cell damage resulting in the detachment of the epidermis from the dermis, followed by exudation of a cell-poor liquid in the space between the detached Figure 10. Dengue rash in the arms and trunk[Lecturer’s PPT]. epidermis and the dermis. This results in blister (vesicle/bulla) formation. MICROSCOPIC PATHOLOGY IN DENGUE FEVER → Blisters are fluid-filled lesions measuring: SMALL BLOOD VESSELS ▪ < or equal to 5mm: Vesicle Endothelial swelling ▪ > 5mm: Bulla Perivascular edema Infiltration with mononuclear inflammatory cells PATHOGENESIS OF HSV INFECTION 1. HSV-1 & HSV-2 LIVER Sites of primary HSV infection: Hepatocellular necrosis with minimal inflammatory → Oral skin/mucosa (Type 1) ❗ response Cause of deficiency of clotting factors in dengue fever → Temporal lobe of the brain (Type 1) → Nongenital skin (Type 1 or 2) → Genital skin (Type 2) → Eye Site of fulminant primary infection: Liver 2. Replicate in skin & mucous membranes at site of entry of the virus (usually oropharynx or genitals) 3. Produce infectious virions 4. Cause vesicular lesions of epidermis & mucous membranes Infects mucoepithelial cells to produce vesicles filled w/ Figure 11. Liver necrosis: (Left) Mid-lobular necrosis and viral particles → progress to pustules → ulcerated or (Right) Focal necrosis of hepatocytes[Lecturer’s PPT]. crusted lesions 5. Spread to sensory neurons which innervate primary sites HEMORRHAGES of replication Seen in gastrointestinal mucosa, skin, pulmonary alveoli, 6. Establish latent infection in the neuronal cell bodies and serosal surfaces PATHOLOGIC FINDINGS IN HSV INFECTION GROSS PATHOLOGY IN HSV INFECTION Fever blisters → AKA Cold sores → Found on facial skin around mucosal orifices (usually around the lips and nose) → Appear as blisters which are intraepithelial vesicles resulting from intracellular edema & ballooning degeneration of epidermal cells ▪ May burst & crust over producing ulcerations Figure 12. Pulmonary hemorrhages within alveoli (yellow arrows) [Lecturer’s PPT]. III. LATENT INFECTIONS Latency is defined as the persistence of viral genomes in cells that do not produce the infectious virus → Latent infections usually caused by herpesviruses Virus causes an acute infection followed by a latent infection in which virus persists in a noninfectious form (dormant state) w/ periodic reactivation & shedding of infectious virus Figure 13. Fever blisters appearing as vesicles. Located Examples of viruses causing latent infections: within/around the lips. (Left: crusting and scab formation of → Herpes simplex virus (HSV) the fever blister)[Lecturer’s PPT]. → Varicella-zoster virus (VZV) Gingivostomatitis ▪ HSV1, HSV2, & VZV: infect epithelial cells & produce → Caused by HSV-1, often seen in children latent infection in postmitotic neurons → Vesicular eruption from the tongue to retropharynx → Cytomegalovirus (CMV) → Causes cervical lymphadenopathy → Epstein-Barr virus (EBV) PATHOLOGY Infectious Diseases I: Viral Infections PAGE 4 of 10  PATHOLOGY | LE 1 Infectious Disease I: Viral infections| Dr. Arlene Santos ❗ Herpetic whitlow → Swollen, erythematous painful lesions of fingers or palm Corneal lesions: clinical finding seen in primary HSV infection of infants and healthcare workers (due to occupational → Two forms: exposure. ▪ Herpes epithelial keratitis − Virus-induced cytolysis of superficial epithelium ▪ Herpes stromal keratitis − Mononuclear cell infiltrate around keratinocytes & endothelial cells − Neovascularization → Scarring → Corneal opacification → eventually resulting to blindness Herpes simplex encephalitis Disseminated skin & visceral herpes infections → in hospitalized patients with cancer or immunosuppression → for immunocompromised patients, any organ may be infected which can be mild or life-threatening → Examples of visceral herpes infections: ▪ Herpes esophagitis Figure 14. Herpetic Whitlow. Swollen, erythematous lesion of ▪ Herpes bronchopneumonia finger[Lecturer’s PPT] ▪ Herpes hepatitis Genital herpes/Herpes Genitalia MICROSCOPIC PATHOLOGY IN HSV INFECTION → More commonly caused by HSV-2 than HSV-1 → Vesicles on genital mucous membranes & external ❗️Cowdry Type A inclusions/ inclusion bodies → Large, pink to purple intranuclear inclusions of HSV genitalia rapidly converted to ulcerations rimmed by infected cells an inflammatory infiltrate ▪ Inclusions consist of viral replication proteins and → Possible fulminating infection in neonates when virions at various stages of assembly that push the infected during passage through the birth canal of an chromatin to the edge of the nucleus. infected mother ▪ Usually caused by HSV-2 ▪ Generalized lymphadenopathy, splenomegaly & necrotic foci throughout lungs, liver, adrenal glands, and CNS Figure 17. HSV vesicle. Cowdry type A inclusion bodies in epithelial cells of the epidermis[Lecturer’s PPT]. Figure 15. Arrows: Genital Herpes vesicles. Located on the genital mucous membranes and external genitalia[Lecturer’s PPT] Figure 18. HSV blister. Arrow: Cowdry type A inclusion Figure 16. Left: HSV vesicle on external genitalia. Right: bodies in HSV-infected cells[Robbins]. HSV vesicle on the buttocks[Lecturer’s PPT]. PATHOLOGY Infectious Diseases I: Viral Infections PAGE 5 of 10 PATHOLOGY | LE 1 Infectious Disease I: Viral infections| Dr. Arlene Santos MICROSCOPIC PATHOLOGY IN CHICKENPOX Intraepithelial vesicle with intranuclear inclusions in the epithelial cells at the base of the vesicle Figure 19. Liver with Herpes hepatitis. Arrows: Cowdry type A inclusion bodies in HSV-infected cells[Lecturer’s PPT]. B. VARICELLA ZOSTER VIRUS (VZV) Figure 22. Microscopic examination of a chickenpox Acute infection with VZV → Chickenpox rash[Lecture PPT]. Reactivation of latent VZV → Shingles/Herpes Zoster Similar to HSV on the following aspects: PATHOLOGIC FINDINGS IN HERPES ZOSTER → Infects mucous membranes, skin & neurons GROSS PATHOLOGY IN HERPES ZOSTER → Causes vesicular skin lesions Presents as a painful dermatomal vesicular rash → Evades immune responses VZV infects the keratinocytes → vesicular skin lesions with → Establishes a latent infection in sensory ganglia intense itching, burning or sharp pain Differs from HSV on: Pain is especially severe with trigeminal nerve → Mode of transmission: through respiratory aerosol involvement → Disseminates hematogenously Rash appears in unilateral dermatomal distribution Latent VZV infection is seen in neurons and/or satellite cells around neurons in the dorsal root ganglia PATHOLOGIC FINDINGS IN CHICKENPOX GROSS PATHOLOGY IN CHICKENPOX The rash occurs approximately 2 weeks after respiratory infection → Initially appears at the trunk → the head & extremities → Lesions progress from macules → vesicles → Resemble “dew drops on a rose petal” Figure 23. Herpes zoster[Lecture PPT]. Herpes Zoster Ophthalmia → Involvement of ophthalmic division of trigeminal nerve or CN V1 in 10-15% of cases Figure 20. Chickenpox[Lecture PPT]. Figure 21. Chickenpox rashes in different locations. (A) Trunk. (B) Hands[Lecture PPT]. Figure 24. Herpes zoster ophthalmia[Lecture PPT]. PATHOLOGY Infectious Diseases I: Viral Infections PAGE 6 of 10 PATHOLOGY | LE 1 Infectious Disease I: Viral infections| Dr. Arlene Santos MICROSCOPIC PATHOLOGY IN HERPES ZOSTER C. CYTOMEGALOVIRUS (CMV) Asymptomatic or mononucleosis-like infection in healthy individuals Devastating systemic infection in neonates and in immunosuppressed Infects different types of cells: → Parenchymal epithelial cells in glandular organs → Neurons in the brain → Alveolar macrophages, epithelial cells & endothelial cells in the lungs → Tubular epithelial & glomerular endothelial cells in the kidney Causes latent infection in monocytes & bone marrow progenitors Can be reactivated when the cellular immunity is depressed Routes of Transmission: → Transplacental (leads to congenital CMV, Cytomegalic Figure 25. Microscopic examination of herpes zoster rash Inclusion Disease) depicting an intraepithelial vesicle [Lecture PPT]. → Neonatal transmission (perinatal CMV) → Genital route (dominant mode of transmission after the age of 15) → Saliva and respiratory secretions → Feco-oral route → Iatrogenic (blood transfusion, organ transplant) PATHOLOGIC FINDINGS IN CMV INFECTION MICROSCOPIC PATHOLOGY IN CMV INFECTION Characteristic enlargement of the infected cells → CMV-infected cells exhibit gigantism of the entire cell (3-4x size of a macrophage) & the nucleus → Presence of large intranuclear basophilic inclusion bodies surrounded by a clear halo (owl's eye) Figure 26. Microscopic examination of herpes zoster (in HPO) showing intranuclear inclusions (at the base of the vesicle) within epithelial cells (blue arrows)[Lecture PPT]. Dorsal root ganglion cell with VZV infection → Ganglion cell necrosis & associated inflammation (predominantly mononuclear inflammatory cells) → Accompanied by herpetic intranuclear inclusions within the neurons and their supporting cells Figure 28. Microscopic section of a lung alveolus containing cells infected by CMV. Note the enlargement of the cell & nucleus, and the intranuclear inclusion bodies surrounded by a clear halo (yellow arrow)[Lecture PPT]. Space intentionally left blank Figure 27. Dorsal root ganglion with VZV infection[Lecture PPT]. PATHOLOGY Infectious Diseases I: Viral Infections PAGE 7 of 10 PATHOLOGY | LE 1 Infectious Disease I: Viral infections| Dr. Arlene Santos Figure 31. Pathologic Findings of CMV [Lecture PPT] Immunocompromised: susceptible to pneumonitis, Figure 29. Characteristic appearance of cells infected by colitis, and severe CMV infections CMV showing “owl’s eye” (blue arrows)[Lecture PPT]. Characteristic gross findings of CMV colitis: → Ulcerations In Figure 29: → Pseudomembrane formation → (A) Lung with CMV-infected cells In Figure 31: → (B) Placenta with a diagnosis of CMV Villitis; → (A) Resected segment of the cecum and ascending ▪ Infection of chorionic villi colon with 2 distinct ulcers which are indicated by the ▪ Inset shows a HPO view of a chorionic villus with white arrows CMV-infected cell → (B) Colon with ulceration (green arrows) ▪ Occurred as a result of transplacental transmission ▪ Histologic findings must be confirmed by positive − A mother with newly acquired or primary CMV immunohistochemistry for CMV infection without antibodies transmits CMV to the ▪ An example of a serologic test for CMV colitis is fetus detecting CMV IgM antibodies which indicate acute infection IV. CHRONIC PRODUCTIVE / PERSISTENT INFECTIONS PATHOGENESIS OF PERSISTENT INFECTIONS In some infections: inability of immune system to eliminate virus and continued viral replication → persistent viremia Examples of viruses which cause chronic infections: → HIV → HBV ▪ High mutation rate of HIV and HBV allows the microorganisms to escape control by the immune system V. TRANSFORMING VIRAL INFECTIONS Figure 30. Neonatal CMV [Lecture PPT] ONCOGENIC VIRUSES Neonatal CMV Viruses implicated in the causation of human cancers → CMV infection acquired during passage through an Can stimulate cell growth & survival by a variety of infected birth canal (cervical or vaginal secretions) or mechanisms from breast milk in mother who does not have protective Examples of oncogenic viruses: EBV, HPV, HBV, and antibodies HTLV-1 → Infected infants develop interstitial pneumonitis, failure to thrive, rash or hepatitis PATHOLOGY Infectious Diseases I: Viral Infections PAGE 8 of 10 PATHOLOGY | LE 1 Infectious Disease I: Viral infections| Dr. Arlene Santos A. EPSTEIN-BARR VIRUS (EBV) GROSS PATHOLOGY IN EBV INFECTION A Herpesvirus which causes infectious mononucleosis Cervical Lymphadenopathy A factor in the development of several human cancers: → Lymph nodes are enlarged in infectious mononucleosis → Nasopharyngeal carcinoma → Commonly involves: → Burkitt lymphoma ▪ Posterior cervical lymph nodes → B cell Non-Hodgkin lymphoma ▪ Axillary lymph nodes → Hodgkin lymphoma ▪ Inguinal lymph nodes Infects the following cells: → Microscopic finding: expansion of paracortical areas → B cells due to activation of the T cells ▪ binds to Complement Receptor 2 (CR2) and causes a latent infection → Oropharyngeal epithelial cells OUTCOME OF EPSTEIN-BARR VIRUS INFECTION Transmitted by close human contact, frequently with the saliva during kissing In immunocompetent hosts: infection is usually asymptomatic or leads to infectious mononucleosis → Characterized by fever, sore throat, generalized lymphadenopathy, splenomegaly, and the appearance of atypical lymphocytes (mononucleosis cells) → Symptoms appear on initiation of host immune response → Cellular immunity mediated by CD8+ cytotoxic T lymphocytes & NK cells In patients with defective cellular immunity: EBV reactivation → uncontrolled proliferation of B cells which may be uncontrolled → EBV-associated B-cell neoplasms. Figure 33. Infectious Mononucleosis-cervical PATHOLOGIC FINDINGS IN EBV INFECTION Lymphadenopathy [Lecture PPT] MICROSCOPIC PATHOLOGY IN EBV INFECTION Severe Pharyngitis Major alterations involve the blood, lymph nodes, spleen, → With diffuse pharyngeal inflammation & tonsillar swelling liver, CNS and occasionally other organs In blood & lymphoid organs: → Absolute Lymphocytosis ▪ Lymphocytes comprise 60% of the total WBCs → 5-80% are atypical lymphocytes ▪ EBV-specific CD8+ cytotoxic T cells ▪ CD16+ NK cells → Reactive proliferation of T cells centered on lymphoid tissues → lymphadenopathy & splenomegaly Liver → Gross finding: hepatomegaly → Histologic findings: ▪ Atypical lymphocytes in portal tracts and sinusoids ▪ Foci of parenchymal necrosis Figure 34.Pathologic Findings in EBV Infection-Pharyngitis [Lecture PPT] DIAGNOSIS OF EBV Depends on the following findings in increasing order of specificity: → Lymphocytosis with atypical lymphocytes in the PBS → A positive heterophile antibody reaction (Monospot test) Figure 32. Normal (L) vs. Atypical Lymphocyte in EBV (R) → A rising titer of specific antibodies for EBV antigens [Lecture PPT] ▪ Includes viral capsid antigens, early antigens or In Figure 32: EBNA (EBV-associated nuclear antigen) → Left: In a normal smear, the RBC is 2/3 the size of a lymphocyte REVIEW QUESTIONS → Right: In EBV infection, there are atypical 1. What is the pathognomonic microscopic finding in lymphocytes which are larger in size, with more measles? cytoplasm, and an oval, indented or folded nucleus a. Koplik Spots ▪ Cytoplasm indented by surrounding RBCs b. Warthin-Finkeldey c. Large germinal centers PATHOLOGY Infectious Diseases I: Viral Infections PAGE 9 of 10 PATHOLOGY | LE 1 Infectious Disease I: Viral infections| Dr. Arlene Santos 2. HSV-1 causes what kind of lesions: giant cells with eosinophilic, nuclear & cytoplasmic a. Oral inclusions. Koplik spots are also pathognomonic, but seen b. Genital macroscopically (gross). Large germinal centers are also a c. Both microscopic finding, but not considered pathognomonic. 3. All of the following viruses are considered oncogenic, 2. C. HSV-1 can be a causative agent of both oral and except: genital lesions. However, it causes oral lesions more a. HIV frequently. On the other hand, HSV-2 is more implicated in b. HBV genital lesions. c. HCV 3. A. HIV produces persistent infections, but is not d. EBV oncogenic. Only EBV, HPV, HTLV-1 & HBV are said to 4. Macroscopic findings in dengue include which of the cause transforming viral infections associated with the following: development of malignancies. a. Conjunctival hemorrhage 4. A. Conjunctival hemorrhage is a macroscopic finding b. Blotchy, brown rashes in dengue including maculopapular rashes. c. Perivascular edema Perivascular edema is a microscopic finding in dengue. d. Koplik spots Blotchy, brown rashes and Koplik spots are macroscopic 5. Which cranial nerve is involved in Herpes Zoster findings in measles. ophthalmia? 5. B. CN V1. Herpes zoster ophthalmia occurs when there is a. CN II involvement of the ophthalmic division of the trigeminal b. CN V1 nerve. c. CN V3 REFERENCES d. CN VII Infectious Disease: Viral Infections- Dr. Arlene Santos (PPT) Batch 2023. (2022). Infectious Disease: Viral Infections [Transcription] ANS: Link to Asynchronous Discussion: 1. B. Warthin Finkeldey cells are the pathognomonic microscopic finding in measles. These are multinucleated PATHOLOGY Infectious Diseases I: Viral Infections PAGE 10 of 10